As diabetes increase medical costs for those affected, research continues to better understand this debilitating disease. Diabetes current research articles focus on various areas of the disease, such as neurogenesis and glucagon response.

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Systems-wide experimental and modeling analysis of insulin signaling through FOXO1 in human adipocytes, normally and in type 2 diabetes

FOXO1 signal regulation may contribute to insulin resistance in fat cells, the most critical type of cell in terms of the development of insulin. In type 2 diabetes, the mechanism of FOXO1 phosphorylation via the mtorc2-mediated phosphorylation of PKB-Ser473 is not affected; however, the cellular abundance of FOXO1 is halved in type 2 diabetes. Phosphorylation of FOXO1 is also stimulated from a crosstalk of the MAPK-branch of insulin.Â The inhibition of mtorc1 with rapamycin reduces FOXO1 levels to the equivalence found in type 2 diabetes in non-diabetic subjects. The diabetic state in human fat cells, therefore, is the result of the reduction of FOXO1 concentration via mtorc1 attenuation, suggesting that the mtorc1-to-IRS1 feedback is a major mechanism of insulin resistance in type 2 diabetes.

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Impaired cognitive function is associated with diabetes, possibly due to defective neurogenesis, of which typically occurs in the dentate gyrus of the hippocampus, the subventricular zone, and the olfactory bulbs. Hypothesizing that olfactory bulb neurogenesis would be affected in diabetes, the study finds that inhibition of Wnt3-induced neurogenesis in the olfactory bulb causes behavioral deficits in steptozotocin-induced diabetic rats such as impaired odor discrimination, cognitive dysfunction, and increased anxiety. GABA and excitatory amino acid transporters of which localize to GABAergic and glutamatergic terminals decreased in the olfactory bulbs of diabetic rats. With the combined data, it is suggested that STZ-induced diabetes affects neurogenesis located in the olfactory bulb via the GABA and glutamate transporter systems. The resultant cause of the affected systems are functional impairments in performance.

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This study compared the effectiveness of angiotensin-converting-enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) in diabetic patients with pre-existing diabetic retinopathy in a large population-based cohort by conducting a propensity score-matched cohort study. The study pulled information from Taiwanâ€™s National Health Insurance Research Database and included adult patients prescribed for either treatment within 90 days after being diagnosed with diabetic retinopathy between 2000 and 2010. ARBS were similar to ACE inhibitors in terms of the risk of major adverse cardiovascular events and all-cause death, as well as other hospital admissions such as acute kidney injury and hyperkalemia. The resultant data lead to the conclusion that ACE inhibitors were similar to ARBs in terms of risk of all-cause death, major adverse cardiovascular events, and other adverse effects among patients with pre-existing diabetic retinopathy.

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Largely mediated by the autonomic nervous system, insulin-induced hypoglycemia is regulated by glucagon, which is produced by the alpha cells in the pancreas. This response is impaired in type 1 diabetes. The focus of this study is to determine if type 1 diabetes patients have an early and severe loss of islet sympathetic nerves as well as testing to see if this nerve loss is permanent, islet-selective, and unobserved in type 2 diabetes. Pancreatic islet and exocrine sympathetic nerve fiber area were quantified in autopsy samples from type 1 and type 2 diabetes patients as well as from a control group possessing no diabetes. The type 1 diabetes sample was found to have a severe loss of islet sympathetic nerves, as opposed to the type 2 diabetic patients of which were observed to have no loss in islet sympathetic nerves. Exocrine sympathetic nerves were not lost in either samples of diabetic patients. Type 1 diabetic patients, therefore, were concluded to have an early, marked, sustained, and islet-selective loss of sympathetic nerves of which may impair the glucagon response to insulin-induced hypoglycemia.

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Insulin clearance may be influenced by the concentration of insulin-degrading enzyme. Decreased insulin-degrading enzyme activity in blood plasma was hypothesized to contributing to hyperinsulinemia and, possibly, type 2 diabetes mellitus as well as obesity. Fasting blood samples from non-obese (BMI<30), obese (BMI>30), and type 2 diabetes patients were obtained, and microvesicular and soluble fractions were isolated from the plasma via ultracentrifugation. Insulin-degrading activity was assayed using trichloracetic acid precipitation, while the enzyme was detected with Western blotting techniques. Although no statistically significant differences were detected in the insulin-degrading enzyme activity of the three groups, the pre-diabetic and diabetic groups displayed a decreasing trend for enzyme activity. In patients receiving insulin treatment, the effect of diabetes was reversed, indicating increased microvesicular degrading activity in comparison to the pre-diabetic group and the diabetic group. The study concluded that insulin-degrading enzymes present in the blood does not significantly contribute to insulin clearance due to the microvesicular fraction showing no insulin clearance unless they were frozen and thawed prior, possibly allowing the microvesicular membranes to rupture releasing the enzyme. Enzymatically active insulin-degrading enzymes are associated with a fraction consistent with exosomes, which may be decreased in pre-diabetic and diabetic patients, and insulin treatment increases microvesicular insulin-degrading enzyme.